Yong-Cai Zhao1, Jun Zhu2, Guang-Yao Song3, Xin-Sheng Li4. 1. Internal Medicine Teaching and Research Room, Hebei Medical University Shijiazhuang 050017, Hebei, China. 2. Department of Laboratory Medicine, University of California San Francisco 94143, CA. 3. Internal Medicine Teaching and Research Room, Hebei Medical University Shijiazhuang 050017, Hebei, China ; Department of Endocrinology, Hebei General Hospital Hebei Province, China. 4. Department of Endocrinology, Cangzhou Central Hospital Cangzhou 061001, Hebei Province, China.
Abstract
AIMS: To study the relationship between thioredoxin-interacting protein (TXNIP) and pancreatic β-cell function in patients with impaired glucose regulation and patients with both impaired glucose regulation and hypertriglyceridemia. METHODS: We analyzed a population of 90 patients with impaired glucose regulation (IGR), 87 patients with IGR and hypertriglyceridemia, and 90 subjects with normal glucose tolerance (NGT). The levels of plasma TXNIP, a regulator of cellular oxidative stress, were measured. The homeostasis model assessment for insulin resistance (HOMA-IR) was used to evaluate insulin resistance in all subjects. In addition, two factors (HOMA for β-cell function [HOMA-β]) and first-phase insulin response [FPIR]) were used to evaluate pancreatic β-cell function. The correlations between the plasma levels of TXNIP, insulin resistance, and islet β-cell dysfunction were analyzed using Pearson's correlation analysis. RESULTS: Compared with NGT, patients with IGR had significantly lower HOMA-β and FPIR, and higher plasma levels of TXNIP. Compared with the IGR group, patients with both IGR and hypertriglyceridemia had significantly lower HOMA-β and FPIR, and higher plasma levels of TXNIP. There was also a negative correlation between TXNIP and HOMA-β or FPIR, and a positive correlation between TXNIP and HOMA-IR. CONCLUSIONS: These data showed that the level of TXNIP is increased in patients with IGR and patients with both IGR and hypertriglyceridemia, islet β-cell dysfunction was related to the increased TXNIP in IGR patients.
AIMS: To study the relationship between thioredoxin-interacting protein (TXNIP) and pancreatic β-cell function in patients with impaired glucose regulation and patients with both impaired glucose regulation and hypertriglyceridemia. METHODS: We analyzed a population of 90 patients with impaired glucose regulation (IGR), 87 patients with IGR and hypertriglyceridemia, and 90 subjects with normal glucose tolerance (NGT). The levels of plasma TXNIP, a regulator of cellular oxidative stress, were measured. The homeostasis model assessment for insulin resistance (HOMA-IR) was used to evaluate insulin resistance in all subjects. In addition, two factors (HOMA for β-cell function [HOMA-β]) and first-phase insulin response [FPIR]) were used to evaluate pancreatic β-cell function. The correlations between the plasma levels of TXNIP, insulin resistance, and islet β-cell dysfunction were analyzed using Pearson's correlation analysis. RESULTS: Compared with NGT, patients with IGR had significantly lower HOMA-β and FPIR, and higher plasma levels of TXNIP. Compared with the IGR group, patients with both IGR and hypertriglyceridemia had significantly lower HOMA-β and FPIR, and higher plasma levels of TXNIP. There was also a negative correlation between TXNIP and HOMA-β or FPIR, and a positive correlation between TXNIP and HOMA-IR. CONCLUSIONS: These data showed that the level of TXNIP is increased in patients with IGR and patients with both IGR and hypertriglyceridemia, islet β-cell dysfunction was related to the increased TXNIP in IGR patients.
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